ArticleCellular & molecular immunology2023
B1-cell-produced anti-phosphatidylserine antibodies contribute to lupus nephritis development via TLR-mediated Syk activation.
Article in Cellular & molecular immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 27 citations in OpenAlex.
- Metabolic determinants of autoimmune kidney diseases.Nature reviews. Nephrology · 2026Review
- B1 Cells for Life.Immunological reviews · 2026Review
- SLA and DDX60L as potential diagnostic biomarkers for subclinical atherosclerosis in systemic lupus erythematosus: a transcriptomic and clinical validation study.Clinical rheumatology · 2026Article
- B1 cells drive pulmonary emphysema progression through ADAM10.Respiratory research · 2026Article
- Lipidome changes indicate oxidative stress, inflammation, and specific loss of glycerophosphoserine inflammatory protection in patients with lupus.Journal of pharmaceutical and biomedical analysis · 2026Article
- Elucidating the Causal Relationships Between B Cells, Dendritic Cells, and Multiple Sclerosis Pathogenesis.Brain and behavior · 2026Article
- [Regulatory effects of mesenchymal stem cells on B1 cells and Tfh cells in children with systemic lupus erythematosus].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026Article
- Dehydrocorydaline treatment suppresses Th17 differentiation via the mTOR-mediated STAT3-RORγt signaling in systemic lupus erythematosus.Molecular medicine (Cambridge, Mass.) · 2026Article
- Major bioactive metabolites derived fromFrontiers in pharmacology · 2026Review
- Do human B-1 lymphocytes truly exist?Frontiers in immunology · 2026Review
- Autoantibody repertoire in lupus nephritis: from pathogenic mechanisms to clinical integration for precision decision-making.Frontiers in immunology · 2026Review
- IL-18 drives the Bhlhe40-mediated pathogenic Th17 cell response and exacerbates autoimmune disease progression.Cellular & molecular immunology · 2025Article
- Distinct autoreactive CD19Nature communications · 2025Article
- Review
- The influence of the gut microbiota on B cells in autoimmune diseases.Molecular medicine (Cambridge, Mass.) · 2025Review
- Age-Associated B Cells in Autoimmune Diseases: Pathogenesis and Clinical Implications.Clinical reviews in allergy & immunology · 2025Review
- Macrophages Unmasked: Their Pivotal Role in Driving Atherosclerosis in Systemic Lupus Erythematosus.Clinical reviews in allergy & immunology · 2025Review
- Anti-PS IgG Immune Complexes Impair Macrophage Phagocytosis in SLE via LOX-Dependent Oxidative Stress.Journal of inflammation research · 2025Article
- The transcription repressor Bach2 is required for maintaining the B-1 cell population by regulating self-renewal.Frontiers in immunology · 2025Article
- Salivary gland transcriptomic analysis and immunophenotyping in the IL-14α transgenic mouse model of Sjögren's disease.Frontiers in dental medicine · 2025Article
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Authors and funding
22 authors at 13 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autoantibodies produced by B cells play a pivotal role in the pathogenesis of systemic lupus erythematosus (SLE). However, both the cellular source of antiphospholipid antibodies and their contributions to the development of lupus nephritis (LN) remain largely unclear. Here, we report a pathogenic role of anti-phosphatidylserine (PS) autoantibodies in the development of LN. Elevated serum PS-specific IgG levels were measured in model mice and SLE patients, especially in those with LN. PS-specific IgG accumulation was found in the kidney biopsies of LN patients. Both transfer of SLE PS-specific IgG and PS immunization triggered lupus-like glomerular immune complex deposition in recipient mice. ELISPOT analysis identified B1a cells as the main cell type that secretes PS-specific IgG in both lupus model mice and patients. Adoptive transfer of PS-specific B1a cells accelerated the PS-specific autoimmune response and renal damage in recipient lupus model mice, whereas depletion of B1a cells attenuated lupus progression. In culture, PS-specific B1a cells were significantly expanded upon treatment with chromatin components, while blockade of TLR signal cascades by DNase I digestion and inhibitory ODN 2088 or R406 treatment profoundly abrogated chromatin-induced PS-specific IgG secretion by lupus B1a cells. Thus, our study has demonstrated that the anti-PS autoantibodies produced by B1 cells contribute to lupus nephritis development. Our findings that blockade of the TLR/Syk signaling cascade inhibits PS-specific B1-cell expansion provide new insights into lupus pathogenesis and may facilitate the development of novel therapeutic targets for the treatment of LN in SLE.
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